Thursday, July 12, 2012

Scaphoid fractures are a huge pitfall in emergency medicine. They can be subtle, and easily missed on the x-ray. If you find any tenderness in the anatomic snuffbox, you need to place a thumb spica splint, and have the patient referred to get a repeat x-ray in 7-10 days.

In a way, the EM approach to the suspected scaphoid fracture is a lot like our approach to the suspected PE. Based on data from the 60s and before, clinicians believe that a disease is difficult to clinically diagnose, radiographically elusive, and requires maximal therapy to avoid devastating outcomes. Some believe that new technologies and tests will provide an solution.

Maybe. But before we try to spend and irradiate our way out of this, let's take a step back, and look at some clinical wisdom you may not have heard about. Research that questions the "conventional wisdom."

And what better fount of conventional wisdom is there, than UpToDate? Let us examine some of the standard clinical advice from the article "Scaphoid Fractures."

Myth 1. Snuffbox tenderness is the cornerstone of diagnosis.
At Yale, there is no shortage of tweed-wearing attendings who solemnly intone rubbish about the decline of the physical exam, about the master diagnosticians of yesteryear, blah, blah, blah...

Cute. Now let's actually look inside.

Hey, you know why we use the ultrasound? Because the physical exams for AAA, CHF, peritoneal blood and gallstones aren't so good, that's why.

Uh, better stop tapping.

Many clinicians cannot recall any other test for scaphoid injury aside from snuffbox tenderness, and this isn't good, because the physical exam is key in determining your clinical suspicion here. This is also a problem since snuffbox tenderness is a lousy test, by itself.

UpToDate, however, assigns it a central role, despite having mentioned other exam techniques (my emphasis):

"Scaphoid fractures are often occult and a high index of suspicion should be maintained for any patient with wrist pain following trauma. Any tenderness in the snuffbox should be treated as a scaphoid fracture until proven otherwise." (UTD)

This is unfortunate advice, since snuffbox tenderness, while usually very sensitive, is utterly non-specific. Parvizi 1998 found it to be only 19% specific, while Pillai 2005 only found 7% specificity! Grover 1996 found 29%, and Freeland 1989 must have had a very light touch, determining a specificity of 40%. This makes the d-dimer look good.

With these shortcomings in mind, there are two other important exam techniques you should know:

Tubercle tenderness - Palpate the bony prominence found on the distal flexor crease of the wrist. It is especially pronounced when the wrist is radially deviated and extended.

These aren't just "nice to know," or for historical interest. They might keep you from needlessly working patients up for fractures they don't have.

For instance, tubercle tenderness can be much more specific for fracture, but just as sensitive, according to Freeland 1989 and Parvizi 1998. Along the same lines, Grover 1996 found that the axial compression test was 80% specific, and 100% sensitive.

Parvizi 1998 found, in fact, that requiring a patient to be positive for all 3 exams would still be perfectly sensitive, while boosting specificity to 74%.

"[Splinting] of symptomatic patients with negative x-rays ... may result in approximately 75 to 90 percent of patients being immobilized for a week or more, [needlessly]." (UTD)

Twenty five percent is a high number, and certainly would justify wrist immobilization if there's any doubt about the diagnosis. It would suggest that radiography is practically useless to detect fractures.

Except that Grover 1996 found that, of the 29 patients who had a scaphoid fracture in their series, all but one was picked up on the initial set of x-rays. Pillai 2005 only had a 7% rate of "occult" scaphoid fracture, while Duncan 1985 saw that none of their 108 patients had an "occult" fracture on follow-up.

So, your mileage may vary, but if both you and the radiologist don't see a fracture, you can feel pretty good about that.

Myth 3. If you don't immobilize the scaphoid soon, there is a huge risk of devastating complications.
The problem with a missed fracture is that non- or mal-union may cause the scaphoid to necrose, which leads to terrible functional outcomes. This is not rare, and it has lead to the perception that immobilization of the wrist needs to take precedence over all other considerations, such as cost, time off from work, and discomfort.

"[N]onunion rates can reach 40 percent when diagnosis and treatment are delayed by four weeks."(UTD)

The reference for this statement, Langhoff 1988, looked at a series of 289 scaphoid fractures. While there was an overall rate of non-union of 3-9%, they found no increase in this rate if the wrist was immobilized up to 28 days following the injury. On the other hand, after 28 days the rate of complications went up. The authors went on to conclude (my emphasis):

"As fractures not visible at the primary X-ray examination were identical with the rest as regards localization and healing characteristics, we assume that these fractures will behave in the same way when subjected to a delay of immobilization of less than four weeks. We therefore consider it unnecessary to immobilize the wrist when there is clinical suspicion of a fracture, but it is not demonstrable at X-ray examination."

They do consider it appropriate to obtain repeat x-rays at 2 weeks if clinical suspicion exists, and forgo immobilization until then.

Myth 4. The presumed scaphoid fracture must be immobilized in a thumb-spica splint.
Well, if my first 2 points are true, this is redundant. But for the sake of argument...

"When a definitive diagnosis cannot be determined at presentation and a scaphoid fracture is suspected on clinical grounds, even if radiographs are negative, the patient should be placed in a thumb spica splint or preferably, a thumb spica cast until a definitive imaging study can be performed." (UTD)

This is a pain in the ass to apply, and probably even worse to wear for the next 10 days, while you try to get into ortho clinic. Good luck using your hand for anything beyond a regal wave.

Hello!

Clay 1991 looked at patients with radiographic fractures, and randomized them to either a "Colles" cast, with the thumb waggling free, or a standard thumb spica.

The nonunion rate was the same in both groups.

Okay, maybe we don't need to immobilize the thumb. But surely we need a hard splint of some sort!

Eh, maybe not. Sjolin 1988 randomized patients with a clinical suspicion for scaphoid fracture, but negative x-rays,, to receive either a dorsal splint (no thumb immobilization) or a "supportive bandage" that could be removed for ADLs.

Everyone got rechecked in 2 weeks, and while there was no difference in complications (all fractures were incomplete or small avulsions), the bandage people were able to go back to work a lot sooner.

Friday, July 6, 2012

When a resident starts interpreting an ECG, listing off features that either suggest or weigh against active ischemia, they will invariably (and properly) mention the deviation in millimeters of ST segments. I will then sanctamoniously intone

If you think I'm smug about ECGs, ask about my thoughts on Huey Lewis.

Despite the my pretentiousness, there is an important element of truth there. (Dr Smith makes this point without smugness, but that's no fun. For me.) If you slavishly follow the standard criteria for STEMI diagnosis on the ECG (with so-and-so number of millimeters in this lead, so many leads with such elevation, etc.), you're going to make a lot of mistakes.

One example is LBBB, a very common etiology of STE on the ECG. Usually, of course, the LBBB is immediately identified, owing to its characteristic appearance, and discussion switches to old vs new, and a review of Sgarbossa vs Smith criteria (peer-reviewed video lecture!).

The Problem with Left Ventricular Hypertrophy

Left ventricular hypertrophy (LVH), however, may not be as obvious, and ED physicians may mistakenly activate the cath lab based on the degree of ST segment elevation. Now, mistakes happen, and we want to have a certain "over-triage" rate, just like surgeons (before the use of CT scanners) had to have a certain "false appendectomy" rate.

LVH, however, is very common, especially in the ED patient population. In fact, LVH is found in about a quarter of the ECGs in the ED that show STE, and is the most common cause.

And it looks like emergency physicians get fooled by LVH fairly often. In one study of cath lab activations, it was found that LVH predicted a "false-postive" result, with an odds ration of 3.1.

How do we keep from getting fooled by this harmless (in the short-term) mimic of STEMI? It isn't simple. Indeed, one recent article suggested that "novice interpreters" of ECGs avoid diagnosing a STEMI in any patient with deep R- or S-waves.

Don't do it!

Well, I hope you are aspiring to more than "novice" status. I also hope that I can provide you some guidance beyond my usual semi-mystical injunctions and platitudes.

Fortunately, there are non-novice ECG interpreters out there who want to share their secrets, like this group out of UC-Davis. The authors used a database ("ACTIVATE-SF) of all the emergency physician-initiated cath lab activations over a period of 3 years in the San Francisco area. This gave a denominator of 411 activations.

Applying any of 3 different scoring systems (Cornell, Sokolow-Lyon, or aVR > 11mm), they found that 79 of these patients met ECG criteria for LVH. Now, some of these patients with LVH ended up having culprit arteries identified at angiography, but most didn't.

They went further, and analyzed this select group of patients who had LVH and a positive cath. They found a few predictors on the ECG.

Certain locations of STE, the degree of STE, and the number of leads with STE all increased the odds of a true STEMI. So did the presence of Q-waves or reciprocal ST depression.

Now, LVH usually only gives you a pseudo-STEMI appearance in the anterior leads, so elevations in the inferior leads, for example, won't cause much confusion. You can see from the table above that STE in the inferior or lateral leads, or a true posterior STEMI, will be easy to distinguish. But what we really care about is trying to distinguish an anterior MI from LVH, and the data above confirms the difficulty; STE in V1-V3 was more often found to not have a culprit artery.

ST Elevation: Absolute and Relative Rather than just measuring the absolute amount of STE, however, the authors also analyzed the relative amount of STE, normalized against the difference of the preceding R- and S-waves.

Here is an illustration of applying this, using an example of LVH without STEMI from the paper:

True STEMIs, overall, had a higher percent STE (25%) versus "false" STEMI (9%). More importantly, if the percent STE < 25%, STEMI was essentially ruled out. If the percent STE > 25%, a STEMI was predicted with a sensitivity of 77%, and 91% specificity.

When they compared this rule, using relative STE, versus the conventional criteria for STEMI that use absolute STE, they found it to be more sensitive and far more specific (73% and 58%, respectively).

Examples For example this patient has LVH, and STE in V1-V3:

But they also have a ratio of STE/(R - S) = 45% STE

Indicating that it's a true STEMI.

Contrast this ECG with this patient with LVH:

They have STE, just like the preceding patient, but a closer look at the anterior leads shows...